Relationships between Psychological Factors and Cardiac Rhythm and Electrical Disturbances Quentin

R. Regestein

M

OST CARDIOLOGISTS feel that cardiac status may somehow wax and wane with psychological fortune, but such speculation rarely proceeds beyond the anecdotal. Engel’ has assembled an impressive number of stories that link sudden death, presumably due to cardiac arrhythmias, with feelings of threat, loss, or even elation. The exacerbations and remissions of cardiac symptoms in the diseased, the ease of obtaining objective measurements via the the moment-to-moment fluctuations of mood and exelectrocardiogram, perience, and the rapidity of cardiac response to mental events all permit inquiry into the relationship between heart and mind. Subjective experience testifies that the heart sensitively reflects emotional state, and experimental evidence corroborates this impression. 2 In the normal individual, under unexceptional circumstances, this relationship between heart and psyche passes for an obvious, if minor, fact of life. Where pathology interferes with the heart’s functioning, flexibility, and optimal capacity to respond under duress, then the influences exerted by aroused mental states may burden rather than merely stimulate the heart. If a man with a mild loss of cardiac reserve becomes overly aroused, it is conceivable that momentary cardiac distress may appear. It is this interaction between pathology in the psychological and the cardiac realms with which this paper is concerned. CARDIAC

STATUS

OF PSYCHIATRIC

PATIENTS

There is evidence that patients with mental disease are more likely to sustain electrocardiographic (EKG) abnormalities than general hospital patients. Heyer et al.3 observed an increased incidence of objectively identifiable EKG aberrations in 200 mental patients. Their study took place in an era that predated the use of major tranquilizers with their untoward cardiac effects. Nor must the psychological derangement be severe enough to require hospitalization for it to be associated with a higher risk of EKG abnormalities. Patients with neurocirculatory asthenia, or what might now be called an anxiety neurosis in an inadequate personality with somatization, are most likely to sustain some EKG abnormality.4 The T-wave changes they often manifest are maximized by adrenalinincreasing activity and are ameliorated by sympatholytic drugs.5 White et a1.6acknowledge a frequency of scattered EKG abnormalities in neurocirculatory asthenia, but find them the result of the asthenic habitus, excitement, and hyperventilation. From the Division of Psychiatry, Department ofMedicine. Peter Bent Brigham Hospital, and rhe Department of Psychiatry, Harvard Medical School, Boston, Mass. Quentin R. Regestein, M.D.: Associate in Medicine (Psychiatryl, Peter Bent Brigham Hospital. Assistant Professor of Psychiatry, Harvard Medical School, Boston, Mass. Requests for reprints should be addressed 10 Q, R. Regestein. M.D., 721 Huntington Ave.. Boston, Mass. 02115. o 1975 by Grune & Stratton, Inc. Comprehensive Psychiatry, Vol. 16. No. 2

(March/April).

1975

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Psychiatrists routinely performing electrocardiograms before administering shock treatment have frequently observed EKG abnormalities. In a series of 193 acutely psychotic, but otherwise healthy males, who averaged 20 years of age, 42% of EKGs demonstrated abnormalities, principally ST-segment and T-wave changes, but also ectopic beats, including 4 cases of nodal or ventricular extrasystoles.’ In another series of 52 young catatonic schizophrenics, similar EKGs were found, as well as a few EKG configurations that fluctuated with the mental status of the patient.* Such transient EKG changes with psychosis have posed practical questions about the advisability of administering shock treatment where no cardiologist was available. g Individuals studying this problem of possible EKG contraindications to shock treatment have concluded that while EKG abnormalities in the severely psychotic population are far more frequent than in the normal population, many of these revert to normal after electroshock treatment.‘-lo It appears that there is no specific causal link between a given type of psychological disorder and any particular type of cardiac arrhythmia. Nevertheless, there seems to be a generally increased risk of rhythm disturbances in patients with psychological troubles of various types. It is as if psychological malfunctioning serves as one possible risk factor predisposing to cardiac arrhythmic disorder. In the studies cited, the mental-hospital population was perhaps more psychopathologically affected than the patients presenting for study in the cardiology clinics, and many of their cardiac disturbances were asymptomatic. This implies that severe mental problems cannot be explained primarily by the presence of cardiac abnormalities.

PSYCHOLOGICAL

STATUS OF CARDIAC

ARRHYTHMIA

PATIENTS

When the reverse study is performed, and the psychological aspects of patients with various cardiac troubles are investigated, an increased incidence of psychological derangement is found. Zauner” detected clinically obvious psychological symptoms in 21 out of 25 patients with very frequent extrasystoles, including symptomatic depressions, manifest anxiety, compulsions, and phobias. He further notes the case of an individual undergoing psychoanalysis who shifted his arrhythmia from paroxysmal atrial tachycardia to multiple extrasystoles, which were subjectively unpleasant. The author postulates some link between the degree to which the patient would allow himself to experience his underlying anxiety and the evolution of his cardiac condition. Sutter et a1.12found that 30 of 48 patients presenting with various types of arrhythmias to a cardiology clinic had no other detectable evidence of organic disease. They called this group “functional.” These patients were more of the hysterical type than the group with further evidence of cardiac disease, which contained an admixture of obsessionals. The first appearance of the rhythmic disorder coincided with serious stress in a surprising majority of patients; in 85% of their population a major stress such as divorce, moving, or death in the family occurred at the onset of the arrhythmia. They proposed that the exact type of EKG abnormality was determined by the type of cardiac rather than mental pathology.

PSYCHOLOGICAL

MORE

FACTORS

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EXTENSIVE

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STUDIES

RHYTHM

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139

FEWER

PATIENTS

The literature cited has sought to deal with the relationship between psychological states and the EKG, but has generally resorted to scanning large numbers of EKG records of patients in given diagnostic categories or even in certain types of institutions. Since mental status fluctuates rapidly, the demonstration of an augmented incidence of EKG abnormalities among the mentally disturbed permits no clear definition of how psychological and nervous system factors influence cardiac behavior. Such studies allow only the most general of conclusions: that a malady of psychological function may lead to a dysfunction of the heart, as assessed by the EKG. Perhaps these studies have been encouraged by the ease of obtaining EKGs under standard conditions in large series of patients. The conditions under which EKGs are obtained, however, may fail to replicate the situations most likely to lead to cardiac disturbances. Furthermore, as emotional factors become more important in our assessment of mental and cardiac states, individual patients, whose emotional idiosyncracies average out in a large series, become more necessary to study. Amid a multi-determinant array of nervous system influences upon the heart, definite explanations for the cardiac behavior caused by such influences become increasingly elusive. It has been known from an earlier era of psychophysiological research that the more complex the emotion, the less clear and more varied are its physiological concomitants.13 Given the individuality of autonomic response,14 the differences in pathophysiological expression of cardiac dysfunction,12 and the uniqueness of any particular psychological make-up, we must survey individual cases to further understand changes in cardiac function as they covary with an individual’s mental state. A few cases taken from the literature document the paroxysmal, episodic nature of cardiac abnormalities as they relate to longitudinally observed mental status. Rahe and ChristI followed an 11-year-old boy with recurrent paroxysmal ventricular tachycardia (VT). Impatience and frustration in this child would bring about high heart rates or prolonged episodes of the VT, but disappointment and sadness would lead to low heart rates and normal sinus rhythm. Crede et al. l6 studied a young man in whom anxiety provoked T-wave changes unrelated to rate, which could be abolished by Amytal and provoked by preparing his arm for venipuncture. This subject also suffered episodes of rapid heart action which could not be reproduced in the laboratory. Benedict and EvansI report studies of an individual whose EKG showed a second degree Wenckebach type of heart block during anxiety attacks. On follow-up l$i years later and after several symptom-free months, the patient showed a prolonged P-R interval of 0.24 sec. They review evidence that alterations in the cardiac conduction mechanism may be frequently associated with anxiety in some patients. Silverman and Goodman18 report on a patient with neurocirculatory asthenia whose P-R interval varied between 0.71 and 0.32 set, depending on his state of anxiety. His EKG showed no Wenckebach phenomenon. Loftus et all9 observed a patient in whom the EKG changes of wandering atria1 pacemaker were regularly observed during manic excitement. Like Rahe and Christ’s boy with VT, only certain specific emotions were associated with the ap-

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pearance of the abnormality. In this case the anomaly was associated with the patient’s episodes of inordinate sexual excitement, but not present during fear or resentment, no matter how intense. These two cases demonstrate the remarkable specificity of emotional state in given individuals which can be associated with cardiac arrhythmias. Evidence for the reversibility of a tendency toward frequent ventricular ectopic activity is supplied by Walker,20 who found in a patient palpitations that began close upon the death of her beloved brother. EKG evidence of frequent ventricular premature beats (VPB’s) and a wandering atria1 pacemaker abruptly ceased after a skillful internist’s interview which induced in the patient a great emotional catharsis and release. Nakamotoal offers a large collection of individual case histories which demonstrate how functional, temporary arrhythmias may vary with the mental state. He associates particular categories of mental distress with specific types of arrhythmic disturbance. VPBs, for instance, supposedly appear during “sudden mental shock” and disappear when the trouble has settled or faded away. While the large number of patients chronically manifesting VPBs would suggest that such classification cannot be generally applied, cases of VPBs presenting with poorly acknowledged grief, described by Walker, provide an example that fits with Nakamoto’s scheme. The particular distress that Nakamoto proposes as provoking the Wenckebach phenomenon in patients is mental and physical exhaustion; after sufficient resolution of the distress, one may occasionally be left with first-degree block. Again the chronic course of many such patients would dispose against this view of the disorder as relapsing and episodic, but, on the other hand, there are few long-term studies relating the life events of the patient with the status of his A-V conduction. Benedict and Evans’ Wenckebach patient was a graduate student who may well have been quite exhausted; his symptoms remitted after 3 weeks of rest and relaxation. He was quite tense upon reexamination lys years later, and yet the EKG showed only first degree block, which Nakamoto mentions as a possible residuum. Arrhythmic activity of many types has been observed to associate with transient psychological events. Wedd and Wilsonz2 report on a 22-year-old mentally retarded boy whose heart usually beat in a nodal rhythm and was prone to periods of ventricular standstill. They discovered that scolding the boy invariably provoked periods of ventricular standstill for 6 or 8 seconds, without changes in respiration or consciousness. Atropine abolished the periods of standstill despite application of previously effective stimuli. TENTATIVE

CONCLUSIONS

The above reports indicate that some relationship can exist between mental status and various cardiac electrical disorders. Unfortunately they also constitute a host of disparate observations whose collation offers some very general and hence vague conclusions. In two cases above, for instance, specific emotional experiences set off arrhythmias. Still others, like sadness or fear, did not. We cannot conceive of emotional factors alone as sufficient causes of functional cardiac derangement. The emotions we have touched upon, anxiety, impatience, grief, exhaustion, etc., are ubiquitous, whereas some of the reported arrhythmias

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141

are rare and therefore not to be explained by these common feelings. Although the various disorders cited proved temporary, rather than permanent, some individual patients, once afflicted, seemed continually to manifest one particular type of cardiac pathology, rather than shifting among various possibilities. Furthermore, reversible cardiac dysfunctions have been reported in patients whose mental state was either rather sound23 or apparently unrelated to their relapsing heart trouble.24 Emotional upset alone would therefore seem neither necessary nor sufficient to provoke cardiac dysfunction. Apparently, fluctuations in mental status may exert a modulating physiological influence, presumably through neural or endocrine pathways, and this influence may, in certain individuals with a pathological disposition to abnormal cardiac function, episodically precipitate arrhythmic crises. One might suspect that heart disease or heart symptoms provoke the anxiety, rather than the reverse, since the heart carries with it universal associations with the basis of life and well-being. Palpitations, for example, may cause the psychological symptoms that the above authors could have misinterpreted as causal to the cardiac disorder. After the mental crisis had abated, however, stigmata of the heart trouble, such as a prolonged P-R interval or the need for drug treatment, continued. In the instances cited, some emotional event, such as grief, being scolded, or impatience, has clearly caused the onset of an arrhythmic episode. Reversible EKG changes have appeared after a traumatic experience, such as accidental killing of a co1league25 or the violent death of a beloved brother.26 Such events make cardiac symptoms unlikely to be the primary cause of the psychological effects seen in connection with them. CASE HISTORIES

We are left with ambiguities in our understanding of how mental status infringes on cardiac rhythm. We know from the above material that arrhythmic episodes do not always depend upon emotional change, but that on occasion they might. In an attempt to further clarify the relationship between psychological factors and cardiac arrhythmias, we interviewed seven patients, consecutively referred with intractable EKG-documented, severe, symptomatic arrhythmic disturbances, in an attempt to gain some more coherent view of the influence of psychological factors upon arrhythmic activity. All patients had relapsing symptomatic episodes, enabling them to provide stories of several situations under which the arrhythmias occurred. Unfortunately, the literature exploring a relationship between psychological events and cardiac arrhythmias was largely written before 24-hr ambulatory EKG monitoring and maximal-exercise EKG testing were used to study arrhythmias. In patients with relapsing arrhythmic disturbances, we were able to use these techniques to more precisely outline cardiac rhythmical and electrical status. Case 1 Mr. C. is a 45-year-old palpitations and weakness less industrious, relatively jobs to escape submission new position required him

refrigeration maintenance technician who sustained his first episode of 1 week after his first change ofjobs in 18 years. He had been working with a incompetent colleague who got promoted through seniority, and changed to someone for whom he had no respect. He kept his anger to himself. His to arrive 3 hr earlier, at 5 a.m. In the first week he could not fall asleep

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easily and became most fatigued. The first symptoms occurred the following Saturday, at 9 a.m. After two cups of Sanka coffee, he experienced palpitations and weakness, relieved by speeding up and walking faster. During the following week, the symptoms would return at 9 a.m. and he would simply abort them by exercising. After a large dinner, the symptoms supervened for a minute on one or two occasions. Chronic problems included anger toward his easygoing adolescent boys and coping with a chronically anxious, depressed, and often angry wife. Exercise EKG revealed atrial premature beats (APBs), early and multifocal ventricular premature beats (VPBs), and mixed arrhythmic activity.

Case 2 Mrs. T. is a 48-year-old housewife who sustained a nearly fatal episode of ventricular fibrillation (VF) while very tired one morning. The previous evening she had entertained many friends who had overstayed their welcome, past midnight, and counseled her to forget work in the morning and sleep instead. Her sense of duty impelled her to arise at 4 a.m. and proceed to the small hospital cafeteria where she comprised the first shift of the day, making breakfast, tending the cash register, clearing tables, and making sandwiches for lunch. She had worked thusly for 2 months, and had constantly applied to the supervisor for more help. She plodded through this particular morning in particular distress, bent down to greet whoever was putting dishes through the low window into the kitchen, and fainted. She was immediately resuscitated by nurses present and carried to the emergency room where she went into VF and was again resuscitated. Subsequent ambulatory EKG monitoring for 24 hr revealed bigeminy, couplets, and VT. Background information revealed that the patient had experienced occasional flutters or sometimes a sudden thump in her chest when arguing with a wayward, delinquent 18-year-old son. The same occurred while talking about him. She misses her 20-year-old daughter, who had left the house 7 months ago to get married. Recently her husband was compelled to stay away during the week to work in another city.

Case 3 Mr. D. has sustained a IO-year history of attacks of atria1 fibrillation (AF). The first had occurred after arising at the unaccustomed hour of 4 a.m. in order to travel to a distant business meeting. He felt very tired during the morning, repaired for two drinks, returned to the meeting and sustained the palpitations, sweating, faintness, and anxiety of his first attack. There is no apparent consistent precipitating circumstance associated with the onset of his attacks. The following conditions increased the likelihood of their onset: (1) a single alcoholic drink, (2) relaxation, e.g., on the occasions when he comes home for lunch and sits down before the television set or when relaxing beside the swimming pool, where he spends his vacations and (3) on first awakening in the morning. The attacks are absent during working hours. He works “in a pressure cooker,” selling liquor on commission and having to push different brands with the constant threat of a supplier withdrawing his company’s exclusive franchise. He maintains a gratifying relationship with his wife, argues with his 21-year-old son about hair length, and feels devoted to an S-year-old adopted daughter. Excitement and exercise do not bring on the attacks.

Case4 Mr. S. is a 48-year-old man whose first arrhythmias began when he awoke from a sound sleep with rapid heart action 2% years prior to assessment. He thought little and did nothing about a few similar attacks during sleep. One day, while at work in a factory stockroom, he experienced the sudden onset of dizziness, sweating, palpitations, and ensuing anxiety, subsequently diagnosed as paroxysmal atria1 fibrillation. Since then he has had 6 attacks. All of these involved moderate beer drinking, 2 of them happened while working strenuously as a handyman, 2 of them happened minutes after the completion of strenuous work, 1 of them came while talking in the company of the family gathered around the kitchen table, and 1 while talking with a friend on the telephone. Twenty-four-hour monitoring revealed multifocal VPBs. Recent history revealed that he had suffered the loss of his father-in-law and boss 5 years ago, and a few weeks thereafter had fallen, injuring himself severely enough to require a back operation and 8

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143

months’ convalescence. He suffered a decline in status and salary, as he lost a lucrative position as salesman in the father-in-law’s now defunct business and was now compelled to hard manual labor.

Case 5 Mr. L. is a 4%year-old man who revealed supraventricular tachycardia with multifocal VPBs when monitored for his first attack of VT 10 years ago. Initial symptoms appeared while playing badminton with his daughter, and he was eventually cardioverted. Since then he has had one attack per year without particular precipitants. Recently he sustained attacks at work. Symptoms have arisen spontaneously while walking, sitting, relaxing, and exercising. Mr. L. presently details his job as a credit-union loan officer. He lives in fear of the angry boss who returns mimeographed copies of small mistakes to him, accompanied by caustic notes, and has fired colleagues after bona fide sick leaves. He obtained the present job through his brothers and fears that, at his age and with a serious heart condition, he will not be hired elsewhere. Meanwhile he continually ruminates about possibly being fired and left destitute. He lives near five of his brothers, three of whom have their own businesses. They lend him money, find him jobs, provide his only social outlets, and even drive him to doctors’ appointments. He and his wife stick to an unexciting routine, watching television, visiting relatives on Saturday night, and taking an occasional weekend drive. He takes pride in a 14-year-old daughter but is disappointed in a 19-year-old son who was talented and thrifty but suddenly dropped out of college and became unemployed.

Case4 Mr. D. is a 46-year-old truck driver who suffered his first myocardial infarction a year before admission to the hospital, and I month after he had been fired from his job of 21 years when the firm was sold. He convalesced for 8 months at home, became increasingly preoccupied and angry with the couple in the same small apartment house who continually fought, and sat at the window swearing at the drug-pushers in the street. After 8 months of this he sustained a second, massive heart attack and recovered in the hospital, but was left with episodic runs of VT, which necessitated frequent readmission. One episode supervened after he had been sitting with his wife drinking a cup of Sanka coffee, and then stood up to prepare for a visit with his brother-in-law who had owned the construction firm for which he had worked many years. The palpitations subsided when he sat down and relaxed for a while, but recurred when he stood up again. A second episode occurred when, while he was lying on a couch watching television, his IO-year-old son came up, lay beside him and put his arm around him. In the hospital, runs of VT were brought on when he was alerted or when his wife appeared.

Case 7 Dr. C. is a 58-year-old dentist with a 50-year history of symptomatic rheumatic valvular disease and a IO-year history of recurrent episodes of acute congestive failure. Five years before presentation, mitral and aortic valve prostheses were installed. The patient has been recently bothered by attacks of AF. Circumstances in which such attacks occurred have been: (1) at the end of a long work day, during which he had been frustrated by several trivial mistakes by his secretary, seated in his laboratory working on a dental prosthesis, (2) the day before Thanksgiving, after a usual day, around midnight, while comfortably seated in a rocking chair, wife seated on his knees, and chatting affectionately, (3) the day after Thanksgiving, lying in bed late at night, watching television, and talking with his wife as he usually does at that time of day, (4) after attending church one evening, upon arriving home and getting out of his car and (5) in the exercise laboratory, on a treadmill provocative test. Circumstances Number 1 and 5 have each provoked two episodes, the other circumstances were each associated with one episode. The patient is an active, extroverted man, interested in several local social organizations, and in bridge and golf. He lived with his parents until age 52, when his mother died, and married, 1year before presentation at age 57, to a pious nurse who was never previously married. She is 15 years younger than he. Previously he had sought brief promiscuities with many sorts of women. He is an overly conscientious man in many areas, cannot free himself from an interest in trivial details, and becomes easily impatient with colleagues. He has assumed much responsibility for planning his own treatment, which has proven mostly successful. He pores over the issues surrounding controversial procedures and the statistics of one surgeon’s performance versus another.

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CASES

Factors that have previously been identified as coronary risk factors, including job dissatisfaction2’ and troubles with relationships at homez8 also appear on our list of background factors for dysrhythmia activity in Table 1. One of our patients, Mr. D., and possibly others may indeed be affected with coronary heart disease. Recent changes in life situations seem frequent, and have also been described as associated with the onset of a number of other disease processes.2g The appearance of severe difficulties with one’s work situation in 5 of 7 subjects, even in this small series, makes employment problems stand out as a particularly important type of stress connected with intractable arrhythmias. No definitive conclusions can be made by examining a small series of patients without comparing them with others suffering analogous diseases. However, we may determine whether our patients fit in with the observations which others have made on such patients. Like the larger series of those with cardiac rhythm disturbances cited,11*12our patients did show a high degree of psychological distress. In many cases, however, the background of mental suffering may have lowered the arrhythmic threshold rather than served as a sufficient cause for the provocation of arrhythmic activity. As indicated in Table 1, the factors which provoked the arrhythmic crises were often mundane and usual, like standing up or having a relaxing cocktail, rather than more dramatic stresses. Of the individual patients presented in the literature, some would episodically regress to a consistent type of arrhythmia, like Rahe and Christ’s boy with VT15 or Wedd and Wilson’s patient with nodal rhythm and occasional asystole.22 Table Patient 1

1. Summary

Arrhythmia APB’s, VPB’s Mixed dysrhythmic

of Patient

Histories

Recent Background

Acute Precipitant

Job and job hours changed activity

Disagreement

with adolescent

Insomnia with fatigue sons

Depressed wife 2

Bigeminy,

couplets,

VT

Job change

Unusual fatigue

VF

Delinquent

adolescent

AF

No recent changes

son

Bending over

Husband out of town during week 3

Fatigue Alcohol Relaxation Upon awakening

4

AF Multifocal

Loss of job status VPB’s

Alcohol work

plus strenuous or just after

strenuous 5

VT

Terrified

of boss

Helplessness 6

VT

Fired after 21 years

in AM

work

Occasionally

exercise

or at work Standing

up

Son hugs him Wife aooears 7

AF

Got married

Fatigue Standing

up

Relaxing

late at night

Exercise

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Other patients would show more than one type of arrhythmic mechanism. The patients in our series varied from patient 3 who demonstrated atrial fibrillation attacks over a lo-year period to several patients who showed mixed dysrhythmic activity during a single EKG monitoring session. We are thus left with the impression that the arrhythmias accompanying symptomatic episodes can be ascertained from previous studies only in some patients. One of the patients had had a myocardial infarction and another had rheumatic heart disease, but no other obvious cardiac pathology underlying the dysrhythmia was detected in the remainder. This relative absence of heart disease is consistent with the previously mentioned literature, in which arrhythmic and electrical abnormalities were present mainly in those who were otherwise free of heart disease. In our small series there did not seem to be any correlation between the type of psychological problem and the type of arrhythmia. The most apparently innocuous behavior, such as bending over, brought on the more serious consequence, ventricular fibrillation. Unusual fatigue appeared to precipitate arrhythmic crisis in four cases. The fatigue was extreme in three of these cases, associated with marked sleep deprivation. To summarize the findings from interviewing 7 patients with intractable arrhythmias: (1) There was a recent supervention of a psychologically important change in the lives of most of the patients. (2) A loss in job or in job status appeared to be a particular risk factor. (3) There was no correlation between overt cardiac pathology and the recurrent arrhythmias. (4) Unusual and extreme fatigue placed individuals at particular risk for an arrhythmic episode. (5) Mundane, trivial behaviors often precipitated episodes, as well as the onset of an emotion-filled moment. DISCUSSION

Our examination of this small population of patients with intractable arrhythmias allows us to consider some impressions imparted by the literature. The large screening studies concluded that some long-term tonic factor induced deviations in cardiac functioning, since a mere diagnosis of neurocirculatory asthenia or schizophrenia or even “mental hospital inpatient” significantly raised one’s chances of finding EKG abnormalities on a single occasion. In our population, there was a strikingly high incidence of severe worsening in some essential aspect of life within a few months before the arrhythmia-related symptoms appeared, confirming the impression of Sutter et al. I2 In contradistinction to some of the other case reports quoted, however, our patients did not develop arrhythmic episodes on the appearance of any particular noxious stimulus; indeed, the most usual and trivial behaviors seemed to be the immediate antecedents of arrhythmic symptoms. We might guess, therefore, that in some patients the long-term background of stress lowers the arrhythmic threshold so much that trivial events, such as standing up, bending over, etc., may, in combination with other physiological factors, elicit a symptomatic episode. Even this model has its exceptions in our series however, in patient 3, Mr. D., whose IO-year history of transient arrhythmic episodes occurred against a background of a relatively stable life and intact mechanisms of coping with it. In fact, relaxation in a chair

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brought on arrhythmias in this man. Our hunch about background stress tonically lowering arrhythmia threshold must therefore remain provisional. Perhaps arrhythmias which emerge in association with bradycardia arise under different psychological situations from those which arise during tachycardia. Unfortunately there are no prospective, long-term studies which would adequately scan for the effect of tonic background events upon the appearance of arrhythmic crises, although there are suggestions that such studies may be valuable (cf. case 10, reference 30). Practicality dictates that laboratory studies use artificiallyinduced anxiety31 among healthy subjects, or inferences about the patient’s psychological status at the moment he happens to be in the laboratory.32 Even assaying cardiological functions of individuals during various fortuitous and real life stresses turns up various abnormalities. 33.34Such methods, however, permit no clear view of the chronic pathophysiological predispositions possibly wrought by ill fortune. Assessing the influence of long-term effects on the heart depends upon the verbal memory of a patient for relevant history. Even if all arrhythmic episodes were symptomatic, cardiac responses to given circumstances may persist long after other behavioral responses to the same circumstances have become extinguished.35 Thus circumstantial data which may be dismissed as meaningless by the patient may nevertheless influence cardiac control mechanisms. Even if memory for .ci’rcumstances previously sufficient to provoke cardiac responses is absent, cardiac’ responses may remain undiminished.3s Therefore, factors of which the patient cannot make the investigator aware may cause abnormal cardiac responses. The investigation of long-term effects upon cardiac functioning are thus rendered extremely difficult. The finding that unusual fatigue anticipated the onset of an arrhythmia in 4 of the patients surprises us. We are unable to explain how fatigue would cause aberrant heart rhythms. In 3 of the subjects, a state of unusual sleeplessness immediately preceded the onset of the first arrhythmic crisis in their lives. It would seem, therefore, that fatigue is somewhat more able to elicit arrhythmic activity in comparison with the many other contingencies of routine experience. Too little is known of how fatigue might affect the many factors stabilizing heart rhythm to allow speculation on this issue. We are left with the impression that a disrupting influence superimposed upon a relatively stable life may provoke some chronically-augmented disposition toward arrhythmia susceptibility, and, while such an alteration is present, that the superimposition of acute events, sometimes emotionally meaningful, sometimes trivial, may be sufficient to provoke an arrhythmic episode. SUMMARY

The paper explores some relationships between psychological state and cardiac electrical and arrhythmic abnormalities. Prior studies of large clinic populations have disclosed an association between such disorders and hospitalizable mental illness. Conversely, some series of cardiology patients have commonly manifested severe psychological symptoms in the setting of even mild or transient cardiac symptoms. Frequently no cardiac disease was found. Careful studies of individual patients demonstrate that emotional arousal, sometimes related to a specific emotion in a given patient, can trigger episodes of serious arrhythmias.

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Seven patients with severe, symptomatic, intractable EKG-documented cardiac arrhythmias were interviewed. Recent changes in job status occurred in 5 patients prior to the first onset of arrhythmias. The immediate precipitants of arrhythmic crises included some emotional experiences, such as a patient’s son hugging him, and some emotionally trivial experiences, such as awakening in the morning or standing up. Severe and unusual fatigue was present in 3 of the patients prior to their first arrhythmic crisis. It was concluded that important events with relatively long-term consequences in an individual’s life may tonically lower the threshold to arrhythmias, and that the short-term effects of a diversity of physiological events (e.g., effort, emotional arousal, relaxation) may interact with the lowered threshold to precipitate an arrhythmic crisis. REFERENCES 1. Engel GL: Sudden and rapid death during psychological stress. Ann Intern Med 74:771782, 1971 2. Cannon WB: Studies of the conditions of activity in the endocrine glands. V. The isolated heart as an indication of adrenal secretion induced by pain, asphyxia and excitement. Am J Physiol50:399-432, 1919 3. Heyer HE, Winans HM, Plessinger VI: Alterations in the form of electrocardiogram in patients with mental disease. Am J Med Sci 214:23~-26, 1947 4. Logue RB, Hanson JF, Knight WA: Electrocardiographic studies in neurocirculatory asthenia. Am Heart J 27:574-577, 1944 5. Wendkos MH, Logue RB: Unstable Twaves in leads II and III in persons with neurocirculatory asthenia. Am Heart J 31:711-723, 1946 6. White PD, Cohen ME, Chapman WP: The electrocardiogram in neurocirculatory asthenia, anxiety neurosis or effort syndrome. Am Heart J 34:390-- 394, 1947 7. Blom GE: A review of electrocardiographic changes in emotional states. J Nerv Ment Dis Il3:233~300, 1951 8. Major S: The electrocardiogram in catatonic schizophrenia. New York J Med 48:14891491, 1948 9. Plice SG, Pfister CW: Electrocardiographic abnormalities in the mentally ill. Illinois Med J99:212-216, 1951 IO. Ruskin A, Ravel J, Beard B: The electrocardiogram in mental disease. Texas Rep Biol Med 51232~245, 1947 I 1. Zauner J: On the role of psychological factors in disturbances of cardiac rhythm. Z Psychosom Med 10:274-276,1964 12. Sutter JM, Gerard R, et al: Psychological factors in cardiac rhythm disorders. Coeur Med Intern 7:293-311, 1968 13. Leschke E: Results and sources of error in

previous studies upon the physiological concomitants of psychological events. Arch f d Ges Psycho1 31:27-37, 1914 14. Lacey JI: Somatic response patterning and stress, in Appley MH, Trimbull R (eds): Psychological Stress. New York, AppletonCentury-Crofts, 1967, pp 14-37 15. Rahe RH, Christ AE: An unusual cardiac (ventricular) arrhythmia in a child. Psychosom Med 28:181-188, 1966 16. Crede RH, Chivers NC, Shapiro AP: Electrocardiographic abnormalities associated with emotional disturbances. Psychosom Med 13:276-288, 1951 17. Benedict RB, Evans JM: Second degree heart block and Wenckebach phenomenon associated with anxietyj Am Heart J 43:626-633, 1952 18. Silverman JJ, Goodman RD: Extraordinary alteration of the P-R interval in neurocirculatory asthenia. Am Heart J 41: 155 160, 195 I 19. Loftus TA, Gold H, Diethelm 0: Cardiac changes in the presence of intense emotion. Am J Psychiatry 101:6977698, 1945 20. Walker cardiovascular 114, 1952

WJ: The patient with functional disorders. Am Heart J 41:109

21, Nakamoto K: cardiac arrhythmias. 1965

Psychogenic paroxysmal Jap Circ J 29:702~ 717,

22. Wedd AM, Wilson DC: Standstill of the heart of vagal origin. Am Heart J 5:493-5Ok 1930 23. Poel W: Cardiometric studies on children. III. Report of a case of incomplete heart block due to vagal effect. Arch Intern Med 69:1040 1050, 1942 24. Levy RC: Partial heart block due to increased vagus action: A case report. Ann Intern Med 12:152551529, 1939 25. Marzahn

H; Clinical

contribution

on the

148

question of functional conduction disturbances. Klin Wochenschr IS:486488,1936 26. Barbera G: On a case of first-degree atrioventricular block of a functional nature. Minerva Med 2:1347-1349,1952 27. Liljefors I, Rahe RH: An identical twin study of psychosocial factors in coronary heart disease in Sweden. Psychosom Med 325233538, 1970 28. Russek HI, Zohman BL: Relative significance of heredity, diet and occupational stress in coronary heart disease of young adults. Am J Med Sci 235266-277.1958 29. Wyler AR, Masuda M, Holmes TH: Magnitude of life events and seriousness of illness. Psychosom Med 33:115-122,197l 30. Stevenson IP, Duncan CH, Wolf S, et al: Life situations, emotions and extrasystoles. Psychosom Med 11:257-272, 1949 31. Hickam, JB, Cargill WH, Golden A: Car-

QUENTIN

R. REGESTEIN

diovascular reactions to emotional stimuli. J Clin Invest 27:29&298, 1948 32. Stevenson IP, Duncan CH, Wolff HG: Circulatory dynamics before and after exercise in patients with and without structural heart disease during anxiety and relaxation. J Clin Invest 28:15341543, 1949 33. Duncan CH, Stevenson IP, Wolff HG: Life situations, emotions and exercise tolerance. Psychosom Med 13:48-50, 1951 34. Mainzer F, Krause M: The influence of fear on the electrocardiogram. Br Heart J 2:221230,194O 35. Wenzel BM: Changes in heart rate associated with responses based on positive and negative reinforcement. J Comp Physiol Psycho1 54:638-644, 1961 36. Hine B, Paolina RM: Retrograde amnesia: Production of skeletal but not cardiac response gradient by electroconvulsive shock. Science 169:12241226, 1970